CORONARY HEMODYNAMICS AND MYOCARDIAL-METABOLISM IN PATIENTS WITH SYNDROME-X - RESPONSE TO PACING STRESS
CORONARY HEMODYNAMICS AND MYOCARDIAL-METABOLISM IN PATIENTS WITH SYNDROME-X - RESPONSE TO PACING STRESS
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DOI：
10.1016/0735-1097(91)90632-j
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发表时间：
1991-06-01
影响因子：
24
通讯作者：
MARZILLI, M
中科院分区：
文献类型：
--
作者：
CAMICI, PG;MARRACCINI, P;MARZILLI, M
对 12 名患有应激性心绞痛和 ST 段压低、冠状动脉造影正常且无痉挛证据（通常标记为 X 综合征）的患者和 10 名正常受试者，评估了静息时和增量心房起搏后的冠状动脉血流动力学、心肌代谢和左心室功能。 在基线研究中，患者和对照受试者的心静脉流量相当。 在起搏过程中，两组患者达到了相同的频率-压力乘积，但患者的频率-压力乘积与心大静脉流量之间的关系斜率明显低于正常受试者（0.0027 vs. 0.0054 ml/mm Hg.beat，p < 0.001）。 尽管如此，两组在休息时（66 +/- 6% vs. 71 +/- 7%，p = NS）和起搏期间（71 +/- 7% vs. 66 +/- 5%，p = NS）的左心室射血分数相当。 在基线研究中，X 综合征患者的心肌葡萄糖提取效率更高（p < 0.05），但丙酮酸和丙氨酸的净心肌交换分别小于和大于对照组。 两组中乳酸的提取程度相似，并且在起搏或恢复期间没有观察到净乳酸释放。 在起搏和恢复期间，X综合征患者表现出净丙酮酸释放，这与净丙酮酸交换呈阳性的对照受试者不同。 此外，X综合征患者在起搏和恢复过程中继续表现出心肌净提取丙氨酸，而正常受试者在整个研究过程中产生丙氨酸。在正常受试者最大起搏期间，心肌碳水化合物氧化显着增加，但在患者中则不然，在患者中，心肌碳水化合物氧化始终低于（p < 0.01）碳水化合物当量（葡萄糖、乳酸、丙酮酸、丙氨酸）的心肌摄取率。 在最大心率-压力乘积水平下，患者的心肌能量消耗显着低于对照受试者（p < 0.01）。因此，尽管可以证明循环底物（葡萄糖、丙酮酸、丙氨酸）净交换的差异，但 X 综合征患者的代谢模式与典型缺血不一致。 因此，在 X 综合征患者中，症状、心电图体征以及起搏期间心大静脉流量增加的损害与保留的整体和局部左心室功能和心肌能量效率共存。
Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects.At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p < 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS).At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p < 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during pacing and recovery, whereas normal subjects produced alanine throughout the study.Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p < 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p < 0.01).The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.